UO SPSY 650 - Developmental-Biopsychosocial Systems Formulation Covering the Life Course

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CHAPTER 17 Alcohol Use and the Alcohol Use Disorders: A Developmental-Biopsychosocial Systems Formulation Covering the Life Course ROBERT A. ZUCKER ALCOHOLISM AND THE ALCOHOL USE DISORDERS 620 HISTORICAL INTRODUCTION AND ISSUES FOR THE FIELD 621 EPIDEMIOLOGY 623 A MULTILEVEL NET FOR DEVELOPMENTAL VARIATION 625 VARIATIONS IN RISK AND COURSE OF THE DISORDER 628 Differences in Alcohol Nonspecific-Risk Structure for Later Disorder Are Present in Early Childhood 629 Heterogeneity in the Course of Risk and Heterogeneity of Nonspecific Risk 632 Heterogeneity of Alcohol-Specific Risk: Prolegomenon to Phenotypic Heterogeneity of Alcohol Use Disorder 635 Heterogeneity of Alcohol Use Disorder and Variations in Course of the DisorderlPhenotype 636 THE OTHER HALF OF THE STORY: ETIOLOGY FROM A NEUROBIOLOGICAL PERSPECTIVE 638 Alcoholism as a Genetic Disorder 638 Intermediate-Level Etiology in Brain 641 Developmental Significance of Neural Models in Late Adolescence 642 OTHER EPIGENETIC ISSUES 643 The Nestedness of Environmental, Behavioral, and Neurobiological Risk 643 Stability and Change in Alcohol Use Disorder Over Time: Factors Predicting Recovery, or Not 644 FUTURE WORK AND CONCLUDING SUMMARY 646 Redefining the Phenotype 646 Is the Child Father to the Man, or Mother to the Woman? Problems in Embracing a Developmental Psychopathology Paradigm 647 Articulating Specific Gene-Brain-Behavior- Environment Relationships 647 Summary and Concluding Remarks 648 REFERENCES 648 ALCOHOLISM AND THE ALCOHOL sociation, 1994) continues that differentiation. I use the USE DISORDERS term AUD when I refer to the umbrella of both, and the dif- ferentiated terminology when issues relating to distin- In 1980, with the advent of the third edition of the guishing features need to be addressed. Diagnostic and Statistical Manual of Mental Disorders (DSM-III; American Psychiatric Association, 1980), Alco- hol Use Disorder rep1aced the broader of Preparation of this chapter was supported by grants from the Na- alcoholism by distinguishing between recurring alcohol use tional institute on ~l~~h~l ~b~~~ and ~l~~h~li~~ (R37 concomitant with problems but lacking tolerance, depend- AA07065, ROI AA12217) and the National Institute on Drug ence, and compulsive alcohol-seeking behavior (alcohol Abuse (R01 DA15398 and U10 DA13710). I am also indebted to abuse) and recurring use with those three characteristics Stephanie Herzberg, Ru Knoedler, and Lisa McLaughlin for present (dependence). DSM-IV (American Psychiatric As- their considerable help in putting this chapter together.Historical Introduction and Issues for the Field 621 HISTORICAL INTRODUCTION AND ISSUES FOR THE FIELD Evidence that alcoholism runs in families has been present in the literature for at least 200 years (Hogarth, 1751; Rush, 1790), but the definitive evidence that this assort- ment had a genetic basis has only gradually accumulated in the past 30 years (Cotton, 1979; R. L. Hall, Hessel- brock, & Stabenau, 1983a, 1983b; McGue, 1994). The landmark study of the modern era that firmly established a heritable basis for the disorder was the adoption study of Donald Goodwin and colleagues (Goodwin, Schulsinger, Knop, Mednick, & Guze, 1973), conducted in Denmark and involving children born to alcoholic and nonalcoholic parents who were adopted away in early life. Although subjected to strong challenges from staunch environmen- talists (Searles, 1988), the Goodwin study and others to follow have repeatedly demonstrated that the disorder has a substantial heritable component (McGue, 1994; McGue, Pickens, & Svikis, 1992; Prescott et a]., 2005). Studies in the early 1980s, most notably that of Cloninger, Bohman, and Sigvardsson (1981) but supported by work from several other groups (Babor et a]., 1992; Hesselbrock et al., 1984; Zucker, 1987), were critical in taking the discourse to another level by provid- ing strong evidence for heterogeneity of the phenotype, with different patterns of heritability, psychiatric comor- bidity, course, and severity found among them. Although this author in 1987 summarized evidence for at least four subtypes, the preponderance or work in the field until quite recently has focused on only two (Babor, 1996; Windle, & Scheidt, 2004). Type I, also called milieu lim- ited by Cloninger (1987), was observed in both men and women and involved adult onset, relatively moderate symptomatology, a low or absent psychiatric comorbidity, and a shorter course. Heritability was mild, and the evi- dence suggested that development of the alcoholic pheno- type was heavily influenced by risk factors in the social environment. Type I1 or male-limited alcoholism was marked by early onset (late adolescence through early adulthood), strong heritability (typically marked by a dense family history, positive pedigree, and passed through the father), severe symptomatology, and aggres- sive/antisocial comorbidity. Later work (Kendler, Heath, Neale, Kessler, & Eaves, 1992; McGue, Pickens, & Svikis, 1992; Pickens et a]., 1991) challenged the male- limited nature of this subtype and demonstrated signifi- cant, albeit lower heritability among women, but continued to show lower transmission of drinking prob- lems and conduct problems. I Although this more recent work conceptually paid trib- ute to the importance of environmental factors in shaping the eventual diagnostic outcome, the dominant perspec- tive was that "alcoholism is a genetic disorder" (National Institute on Alcohol Abuse and Alcoholism, 1985), and the conceptualization of the epigenesis of the disorder was a heavily bottom-up model. In fact, one prominent genetic researcher of that era made the assertion as recently as 5 years ago that environmental factors would only be important after the "alcoholism" genes were discovered, at which time the manner in which the social environment moderated their expression would be of scientific and preventive interest. Social and psychological influences were viewed as risk factors for drinking behavior and drinking problems in adolescence, but their potential im- pact on developmentally later clinical-level phenomena was discounted (cf. Fillmore et al., 1991; Zucker & Gomberg, 1986). In contrast, the dominant scientific paradigm for under- standing


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UO SPSY 650 - Developmental-Biopsychosocial Systems Formulation Covering the Life Course

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